Alpha-enolase regulates the malignant phenotype of pulmonary artery smooth muscle cells via the AMPK-Akt pathway

Dai, Jingbo; Zhou, Qingwen; Chen, Jiwang; Rexius‐Hall, Megan L.; Rehman, Jalees; Zhou, Guofei

doi:10.1038/s41467-018-06376-x

Cited by 107 publications

(94 citation statements)

References 63 publications

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“…17,[19][20][21][22]25,26 The present research described above also confirmed that ENO1 is highly expressed in chemoresistant SCLC cells. 17,[19][20][21][22]25,26 The present research described above also confirmed that ENO1 is highly expressed in chemoresistant SCLC cells.…”

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

“…Increasing evidence has shown that ENO1 can function as an oncogenic protein by promoting cell proliferation, invasion and metastasis in many cancers. 17,[19][20][21][22]25,26 The present research described above also confirmed that ENO1 is highly expressed in chemoresistant SCLC cells. To examine whether ENO1 promotes chemoresistance of SCLC, we knocked down its expression in chemoresistant SCLC cells and then analysed drug resistance.…”

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

“…17 In tumours, ENO1 is overexpressed and activated, which enhances the glycolytic process. 22 More importantly, some lncRNAs and proteins have been reported to interact with ENO1 to regulate its expression or activity in tumours. [19][20][21] In addition, ENO1 can regulate the malignant biological functions of pulmonary artery smooth muscle cells through the AMPK/Akt signalling pathway.…”

Section: Introductionmentioning

confidence: 99%

“…[19][20][21] In addition, ENO1 can regulate the malignant biological functions of pulmonary artery smooth muscle cells through the AMPK/Akt signalling pathway. 22 More importantly, some lncRNAs and proteins have been reported to interact with ENO1 to regulate its expression or activity in tumours. 19,23,24 This study is the first to show that FGFRL1 is involved in SCLC.…”

Section: Introductionmentioning

confidence: 99%

“…Then, we confirmed that FGFRL1 interacts with ENO1 in SCLC cells by reverse Co-IP and immunofluorescence assays.ENO1 is a glycolytic enzymes involved in certain key biological process in tumorigenesis, proliferation, migration and invasion of cancer. 23 ENO1 catalyses the dehydration of 2-PG to PEP during glycolysis22 and acts as a positive regulator of the PI3K/Akt pathway. Some studies have reported that lncRNAs or proteins can interact with ENO1 and affect its expression or activity in tumours.Chen et al 19 demonstrated that WW domain-binding protein 2 interacts with ENO1 and affects its expression.…”

mentioning

confidence: 99%

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FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

Chen

Zheng

et al. 2020

J Cellular Molecular Medi

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Fibroblast growth factor receptor-like 1 (FGFRL1), a member of the FGFR family, has been demonstrated to play important roles in various cancers. However, the role of FGFRL1 in small-cell lung cancer (SCLC) remains unclear. Our study aimed to investigate the role of FGFRL1 in chemoresistance of SCLC and elucidate the possible molecular mechanism. We found that FGFRL1 levels are significantly up-regulated in multidrug-resistant SCLC cells (H69AR and H446DDP) compared with the sensitive parental cells (H69 and H446). In addition, clinical samples showed that FGFRL1 was overexpressed in SCLC tissues, and high FGFRL1 expression was associated with the clinical stage, chemotherapy response and survival time of SCLC patients. Knockdown of FGFRL1 in chemoresistant SCLC cells increased chemosensitivity byincreasing cell apoptosis and cell cycle arrest, whereas overexpression of FGFRL1 in chemosensitive SCLC cells produced the opposite results. Mechanistic investigations showed that FGFRL1 interacts with ENO1, and FGFRL1 was found to regulate the expression of ENO1 and its downstream signalling pathway (the PI3K/Akt pathway) in SCLC cells. In brief, our study demonstrated that FGFRL1 modulates chemoresistance of SCLC by regulating the ENO1-PI3K/Akt pathway. FGFRL1 may be a predictor and a potential therapeutic target for chemoresistance in SCLC. K E Y W O R D Schemoresistance, ENO1, FGFRL1, PI3K/Akt pathway, small-cell lung cancer

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Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

Chen

Zheng

et al. 2020

J Cellular Molecular Medi

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The effects of sodium–glucose cotransporter 2 inhibitors on the ‘forgotten’ right ventricle

Qu,

Duan,

Chen

2024

ESC Heart Failure

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With the progress in diagnosis, treatment and imaging techniques, there is a growing recognition that impaired right ventricular (RV) function profoundly affects the prognosis of patients with heart failure (HF), irrespective of their left ventricular ejection fraction (LVEF). In addition, right HF (RHF) is a common complication associated with various diseases, including congenital heart disease, myocardial infarction (MI), pulmonary arterial hypertension (PAH) and dilated cardiomyopathy (DCM), and it can manifest at any time after left ventricular assist devices (LVADs). The sodium–glucose cotransporter 2 (SGLT2) inhibition by gliflozins has emerged as a cornerstone medicine for managing type 2 diabetes mellitus (T2DM) and HF, with an increasing focus on its potential to enhance RV function. In this review, we aim to present an updated perspective on the pleiotropic effects of gliflozins on the right ventricle and offer insights into the underlying mechanisms. We can ascertain their advantageous impact on the right ventricle by discussing the evidence obtained in animal models and monumental clinical trials. In light of the pathophysiological changes in RHF, we attempt to elucidate crucial mechanisms regarding their beneficial effects, including alleviation of RV overload, reduction of hyperinsulinaemia and inflammatory responses, regulation of nutrient signalling pathways and cellular energy metabolism, inhibition of oxidative stress and myocardial fibrosis, and maintenance of ion balance. Finally, this drug class's potential application and benefits in various clinical settings are described, along with a prospective outlook on future clinical practice and research directions.

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NLRC3 inhibits PDGF‐induced PASMCs proliferation via PI3K‐mTOR pathway

Zha

Zhou

Tan

et al. 2020

Journal Cellular Physiology

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Few studies about nucleotide‐oligomerization domain‐like receptor subfamily C3 (NLRC3) in PASMCs have been conducted. This research aimed to investigate the role of NLRC3 on platelet‐derived growth factor (PDGF)‐induced proliferation of pulmonary artery smooth muscle cells (PASMCs) and its underlying mechanism. We found that the proliferation of PASMCs stimulated with PDGF decreased when phosphoinositide 3‐kinase (PI3K) or mammalian target of rapamycin (mTOR) inhibitors pretreatment. Overexpression of NLRC3 inhibited the proliferation of PASMCs and the phosphorylation of PI3K and mTOR while knocking down NLRC3 reversed this effect. Targeted to PI3K or mTOR can also reverse the effect of NLRC3. Activation of PI3K increased the phosphorylation of mTOR while inhibition of PI3K reduced it. Our data suggest that PDGF can induce abnormal proliferation of PASMCs, and NLRC3 suppresses activation of the PI3K‐mTOR signaling thus inhibits PASMCs proliferation. These findings unveiled the effect of NLRC3 as an inhibitor of the PI3K‐mTOR pathway mediating protection against PASMCs proliferation.

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Alpha-enolase regulates the malignant phenotype of pulmonary artery smooth muscle cells via the AMPK-Akt pathway

Cited by 107 publications

References 63 publications

FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

The effects of sodium–glucose cotransporter 2 inhibitors on the ‘forgotten’ right ventricle

NLRC3 inhibits PDGF‐induced PASMCs proliferation via PI3K‐mTOR pathway

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